Validation of the mean systemic filling pressure assessment with preserved arterial blood flow by comparing two methods of calculation.
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ABSTRACT:
SUBMITTER: De Blasi RA
PROVIDER: S-EPMC8338930 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Venous return is the flow of blood from the systemic venous network towards the right heart. At steady state, venous return equals cardiac output, as the venous and arterial systems operate in series. However, unlike the arterial one, the venous network is a capacitive system with a high compliance. It includes a part of unstressed blood, which is a reservoir that can be recruited via sympathetic endogenous or exogenous stimulation. Guyton's model describes the three determinants of venous return: the mean systemic filling pressure, the right atrial pressure and the resistance to venous return. Recently, new methods have been developed to explore such determinants at the bedside. In this narrative review, after a reminder about Guyton's model and current methods used to investigate it, we emphasize how Guyton's physiology helps understand the effects on cardiac output of common treatments used in critically ill patients.
| S-EPMC9128096 | biostudies-literature
Project description:The bedside hemodynamic assessment of the critically ill remains challenging since blood volume, arterial-venous interaction and compliance are not measured directly. Mean circulatory filling pressure (Pmcf) is the blood pressure throughout the vascular system at zero flow. Animal studies have shown Pmcf provides information on vascular compliance, volume responsiveness and enables the calculation of stressed volume. It is now possible to measure Pmcf at the bedside. We performed a systematic review of the current Pmcf measurement techniques and compared their clinical applicability, precision, accuracy and limitations. A comprehensive search strategy was performed in PubMed, Embase and the Cochrane databases. Studies measuring Pmcf in heart-beating patients at the bedside were included. Data were extracted from the articles into predefined forms. Quality assessment was based on the Newcastle-Ottawa Scale for cohort studies. A total of 17 prospective cohort studies were included. Three techniques were described: Pmcf hold, based on inspiratory hold-derived venous return curves, Pmcf arm, based on arterial and venous pressure equilibration in the arm as a model for the entire circulation, and Pmcf analogue, based on a Guytonian mathematical model of the circulation. The included studies show Pmcf to accurately follow intravascular fluid administration and vascular compliance following drug-induced hemodynamic changes. Bedside Pmcf measures allow for more direct assessment of circulating blood volume, venous return and compliance. However, studies are needed to determine normative Pmcf values and their expected changes to therapies if they are to be used to guide clinical practice.
| S-EPMC6010367 | biostudies-literature
Project description:Mean systemic filling pressure (Pms) is a promising parameter in determining intravascular fluid status. Pms derived from venous return curves during inspiratory holds with incremental airway pressures (Pms-Insp) estimates Pms reliably but is labor-intensive. A computerized algorithm to calculate Pms (Pmsa) at the bedside has been proposed. In previous studies Pmsa and Pms-Insp correlated well but with considerable bias. This observational study was performed to validate Pmsa with Pms-Insp in cardiac surgery patients. Cardiac output, right atrial pressure and mean arterial pressure were prospectively recorded to calculate Pmsa using a bedside monitor. Pms-Insp was calculated offline after performing inspiratory holds. Intraclass-correlation coefficient (ICC) and assessment of agreement were used to compare Pmsa with Pms-Insp. Bias, coefficient of variance (COV), precision and limits of agreement (LOA) were calculated. Proportional bias was assessed with linear regression. A high degree of inter-method reliability was found between Pmsa and Pms-Insp (ICC 0.89; 95%CI 0.72-0.96, p = 0.01) in 18 patients. Pmsa and Pms-Insp differed not significantly (11.9 mmHg, IQR 9.8-13.4 vs. 12.7 mmHg, IQR 10.5-14.4, p = 0.38). Bias was -0.502 ± 1.90 mmHg (p = 0.277). COV was 4% with LOA -4.22 - 3.22 mmHg without proportional bias. Conversion coefficient Pmsa ➔ Pms-Insp was 0.94. This assessment of agreement demonstrates that the measures Pms-Insp and the computerized Pmsa-algorithm are interchangeable (bias -0.502 ± 1.90 mmHg with conversion coefficient 0.94). The choice of Pmsa is straightforward, it is non-interventional and available continuously at the bedside in contrast to Pms-Insp which is interventional and calculated off-line. Further studies should be performed to determine the place of Pmsa in the circulatory management of critically ill patients. ( www.clinicaltrials.gov ; TRN NCT04202432, release date 16-12-2019; retrospectively registered).Clinical Trial Registration www.ClinicalTrials.gov , TRN: NCT04202432, initial release date 16-12-2019 (retrospectively registered).
| S-EPMC8011774 | biostudies-literature
Project description:Background: A decade ago, it became possible to derive mean systemic filling pressure (MSFP) at the bedside using the inspiratory hold maneuver. MSFP has the potential to help guide hemodynamic care, but the estimation is not yet implemented in common clinical practice. In this study, we assessed the ability of MSFP, vascular compliance (Csys), and stressed volume (Vs) to track fluid boluses. Second, we assessed the feasibility of implementation of MSFP in the intensive care unit (ICU). Exploratory, a potential difference in MSFP response between colloids and crystalloids was assessed. Methods: This was a prospective cohort study in adult patients admitted to the ICU after cardiac surgery. The MSFP was determined using 3-4 inspiratory holds with incremental pressures (maximum 35 cm H2O) to construct a venous return curve. Two fluid boluses were administered: 100 and 500 ml, enabling to calculate Vs and Csys. Patients were randomized to crystalloid or colloid fluid administration. Trained ICU consultants acted as study supervisors, and protocol deviations were recorded. Results: A total of 20 patients completed the trial. MSFP was able to track the 500 ml bolus (p < 0.001). In 16 patients (80%), Vs and Csys could be determined. Vs had a median of 2029 ml (IQR 1605-3164), and Csys had a median of 73 ml mmHg-1 (IQR 56-133). A difference in response between crystalloids and colloids was present for the 100 ml fluid bolus (p = 0.019) and in a post hoc analysis, also for the 500 ml bolus (p = 0.010). Conclusion: MSFP can be measured at the bedside and provides insights into the hemodynamic status of a patient that are currently missing. The clinical feasibility of Vs and Csys was judged ambiguously based on the lack of required hemodynamic stability. Future studies should address the clinical obstacles found in this study, and less-invasive alternatives to determine MSFP should be further explored. Clinical Trial Registration: ClinicalTrials.gov Identifier NCT03139929.
| S-EPMC9745184 | biostudies-literature
Project description:ObjectivesLongitudinal hemodynamic follow-up is important in the management of pulmonary hypertension (PH). This study aimed to evaluate the potential of MR 4-dimensional (4D) flow imaging to predict changes in the mean pulmonary arterial pressure (mPAP) during serial investigations.MethodsForty-four adult patients with PH or at risk of developing PH repeatedly underwent routine right heart catheterization (RHC) and near-term MR 4D flow imaging of the main pulmonary artery. The duration of vortical blood flow along the main pulmonary artery was evaluated from MR 4D velocity fields using prototype software and converted to an MR 4D flow imaging-based mPAP estimate (mPAPMR) by a previously established model. The relationship of differences between RHC-derived baseline and follow-up mPAP values (ΔmPAP) to corresponding differences in mPAPMR (ΔmPAPMR) was analyzed by means of regression and Bland-Altman analysis; the diagnostic performance of ΔmPAPMR in predicting mPAP increases or decreases was investigated by ROC analysis.ResultsAreas under the curve for the prediction of mPAP increases and decreases were 0.92 and 0.93, respectively. With the natural cutoff ΔmPAPMR = 0 mmHg, mPAP increases (decreases) were predicted with an accuracy, sensitivity, and specificity of 91% (91%), 85% (89%), and 94% (92%), respectively. For patients in whom 4D flow allowed a point estimate of mPAP (mPAP > 16 mmHg), ΔmPAPMR correlated strongly with ΔmPAP (r = 0.91) and estimated ΔmPAP bias-free with a standard deviation of 5.1 mmHg.ConclusionsMR 4D flow imaging allows accurate non-invasive prediction and quantification of mPAP changes in adult patients with PH or at risk of developing PH.Trial registrationClinicalTrials.gov identifier: NCT00575692 and NCT01725763 KEY POINTS: • MR 4D flow imaging allows accurate non-invasive prediction of mean pulmonary arterial pressure increases and decreases in adult patients with or at risk of developing pulmonary hypertension. • In adult patients with mean pulmonary arterial pressure > 16 mmHg, MR 4D flow imaging allows estimation of longitudinal mean pulmonary arterial pressure changes without bias with a standard deviation of 5.1 mmHg.
| S-EPMC7979582 | biostudies-literature
Project description:BackgroundIn randomized clinical controlled trials, the choice of usual care as the comparator may be associated with better clinician uptake of the study protocol and lead to more generalizable results. However, if care processes evolve to resemble the intervention during the course of a trial, differences between the intervention group and usual care control group may narrow. We evaluated the effect on mean arterial pressure of an unblinded trial comparing a lower mean arterial pressure target to reduce vasopressor exposure, vs. a clinician-selected mean arterial pressure target, in critically ill patients at least 65 years old.MethodsFor this multicenter observational study using data collected both prospectively and retrospectively, patients were recruited from five of the seven trial sites. We compared the mean arterial pressure of patients receiving vasopressors, who met or would have met trial eligibility criteria, from two periods: [1] at least 1 month before the trial started, and [2] during the trial period and randomized to usual care, or not enrolled in the trial.ResultsWe included 200 patients treated before and 229 after trial initiation. There were no differences in age (mean 74.5 vs. 75.2 years; p = 0.28), baseline Acute Physiology and Chronic Health Evaluation II score (median 26 vs. 26; p = 0.47) or history of chronic hypertension (n = 126 [63.0%] vs. n = 153 [66.8%]; p = 0.41). Mean of the mean arterial pressure was similar between the two periods (72.5 vs. 72.4 mmHg; p = 0.76).ConclusionsThe initiation of a trial of a prescribed lower mean arterial pressure target, compared to a usual clinician-selected target, was not associated with a change in mean arterial pressure, reflecting stability in the net effect of usual clinician practices over time. Comparing prior and concurrent control groups may alleviate concerns regarding drift in usual practices over the course of a trial or permit quantification of any change.
| S-EPMC8722048 | biostudies-literature
Project description:Background Even a small change in the pressure gradient between the venous system and the right atrium can have significant hemodynamic effects. Mean systemic filling pressure (MSFP) is the driving force of the venous system. As a result, MSFP has a significant effect on cardiac output. We aimed to test the hypothesis that the hemodynamic instability during induction of general anesthesia by intravenous propofol administration is caused by changes in MSFP. Methods We prospectively collected data from 15 patients undergoing major surgery requiring invasive hemodynamic monitoring. Hemodynamic parameters, including MSFP, were measured before and after propofol administration and following intubation, using venous return curves at a no-flow state induced by a pneumatic tourniquet. Results A significant decrease in MSFP was observed in all study patients after propofol administration (median (IQR) pressure 17 (9) mmHg compared with 25 (7) before propofol administration, p = 0.001). The pressure gradient for venous return (MSFP – central venous pressure; CVP) also decreased following propofol administration from 19 (8) to 12 (6) mmHg, p = 0.001. Central venous pressure did not change. Conclusions These results support the hypothesis that induction of anesthesia with propofol causes a marked reduction in MSFP. A possible mechanism of propofol-induced hypotension is reduction in preload due to a decrease in the venous vasomotor tone. Supplementary Information The online version contains supplementary material available at 10.1186/s12871-022-01773-8.
| S-EPMC9306094 | biostudies-literature
Project description:BACKGROUND:HVAD left ventricular assist device flow waveforms provides graphical real-time information linking device performance with invasive hemodynamics. Previous studies have demonstrated a good correlation between the slopes of the ventricular filling phase slope (VFPS) and directly measured pulmonary capillary wedge pressure (PCWP). We aimed to validate the utility of VFPS to estimate PCWP and predict clinical outcomes. METHODS:In this prospective blinded study, screenshots from the HVAD monitor and simultaneous invasive hemodynamic measurements were obtained. Each screenshot was digitized and the VFPS was calculated by 2 independent reviewers who were blinded to the hemodynamic results. The equation PCWP?=?7.053 +1.365?×?(VFPS) was derived from a previously published dataset and the estimated PCWP was correlated to the actually measured PCWP. RESULTS:One hundred thirty-one sets of simultaneous measurements (VFPS and PCWP) were obtained from 27 HVAD patients (mean age 55 years, 47% male). A previously proposed cutoff of VFPS ?5.8 L/min/s predicted PCWP ? 18 mmHg with 91.5% sensitivity and 95.2% specificity with the area under curve of 0.987. The estimated PCWP significantly correlated with measured PCWP (R2?=?0.65, P < .001) and showed acceptable agreement with measured PCWP. Patients with VFPS ? 5.8 L/min/s experienced significantly higher heart failure readmission rates than those without (0.24 vs 0.05 events/y, P < .001). CONCLUSIONS:VFPS of the HVAD flow waveform is a novel noninvasive parameter that can estimate PCWP.
| S-EPMC7347084 | biostudies-literature
Project description:PurposeCerebral blood flow (CBF) needs to be precisely controlled to maintain brain functions. While previously believed to be autoregulated and near constant over a wide blood pressure range, CBF is now understood as more pressure passive. However, there are still questions regarding the integrated nature of CBF regulation and more specifically the role of cardiac output. Our aim was, therefore, to explore the effects of MAP and cardiac output on CBF in a combined model of reduced preload and increased afterload.Method16 healthy volunteers were exposed to combinations of different levels of simultaneous lower body negative pressure and isometric hand grip. We measured blood velocity in the middle cerebral artery (MCAV) and internal carotid artery (ICAV) by Doppler ultrasound, and cerebral oxygen saturation (ScO2) by near-infrared spectroscopy, as surrogates for CBF. The effect of changes in MAP and cardiac output on CBF was estimated with mixed multiple regression.ResultBoth MAP and cardiac output had independent effects on MCAV, ICAV and ScO2. For ICAV and ScO2 there was also a statistically significant interaction effect between MAP and cardiac output. The estimated effect of a change of 10 mmHg in MAP on MCAV was 3.11 cm/s (95% CI 2.51-3.71, P < 0.001), and the effect of a change of 1 L/min in cardiac output was 3.41 cm/s (95% CI 2.82-4.00, P < 0.001).ConclusionThe present study indicates that during reductions in cardiac output, both MAP and cardiac output have independent effects on CBF.
| S-EPMC8260418 | biostudies-literature
Project description:Objective: Distributed models of the arterial tree allow studying the effect of physiological and pathophysiological changes in the vasculature on hemodynamics. For the adult, several models exist; however, a model encompassing the full age range from newborn to adult was until now lacking. Our goal is to describe a complete distributed hemodynamic model for normal development from newborn to adult. Methods: The arterial system was modeled by 121 segments characterized by length, radius, wall thickness, wall stiffness, and wall viscosity. The final segments ended in three-element Windkessels. All parameters were adapted based on body height and weight as a function of age as described in the literature. Results: Pressures and flows are calculated as a function of age at sites along the arterial tree. Central to peripheral transfer functions are given. Our results indicate that peripheral pressure in younger children resembles central pressure. Furthermore, total arterial compliance, inertance and impedance are calculated. Findings indicate that the arterial tree can be simulated by using a three-element Windkessel system. Pulse wave velocity in the aorta was found to increase during development. Conclusions: The arterial system, modeled from newborn to adult bears clinical significance, both for the interpretation of peripheral measured pressure in younger and older children, and for using a Windkessel model to determine flow from pressure measurements.
| S-EPMC7248228 | biostudies-literature